The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer via autophagy
Identifieur interne : 000117 ( Pmc/Curation ); précédent : 000116; suivant : 000118The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer via autophagy
Auteurs : Ji Wang ; Shuduo Xie ; Jingjing Yang ; Hanchu Xiong ; Yunlu Jia ; Yulu Zhou ; Yongxia Chen ; Xiaogang Ying ; Cong Chen ; Chenyang Ye [République populaire de Chine] ; Linbo Wang ; Jichun ZhouSource :
- Journal of Hematology & Oncology [ 1756-8722 ] ; 2019.
Abstract
Tamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.
Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.
In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.
Our findings demonstrate that H19 induces autophagy activation
The online version of this article (10.1186/s13045-019-0747-0) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13045-019-0747-0
PubMed: 31340867
PubMed Central: 6657081
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer <italic>via</italic>
autophagy</title>
<author><name sortKey="Wang, Ji" sort="Wang, Ji" uniqKey="Wang J" first="Ji" last="Wang">Ji Wang</name>
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<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Xie, Shuduo" sort="Xie, Shuduo" uniqKey="Xie S" first="Shuduo" last="Xie">Shuduo Xie</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Yang, Jingjing" sort="Yang, Jingjing" uniqKey="Yang J" first="Jingjing" last="Yang">Jingjing Yang</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Xiong, Hanchu" sort="Xiong, Hanchu" uniqKey="Xiong H" first="Hanchu" last="Xiong">Hanchu Xiong</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Jia, Yunlu" sort="Jia, Yunlu" uniqKey="Jia Y" first="Yunlu" last="Jia">Yunlu Jia</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Zhou, Yulu" sort="Zhou, Yulu" uniqKey="Zhou Y" first="Yulu" last="Zhou">Yulu Zhou</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chen, Yongxia" sort="Chen, Yongxia" uniqKey="Chen Y" first="Yongxia" last="Chen">Yongxia Chen</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Ying, Xiaogang" sort="Ying, Xiaogang" uniqKey="Ying X" first="Xiaogang" last="Ying">Xiaogang Ying</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chen, Cong" sort="Chen, Cong" uniqKey="Chen C" first="Cong" last="Chen">Cong Chen</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Ye, Chenyang" sort="Ye, Chenyang" uniqKey="Ye C" first="Chenyang" last="Ye">Chenyang Ye</name>
<affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Cancer Institute (Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Second Affiliated Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
Hangzhou, 310009 China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Hangzhou</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Wang, Linbo" sort="Wang, Linbo" uniqKey="Wang L" first="Linbo" last="Wang">Linbo Wang</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Zhou, Jichun" sort="Zhou, Jichun" uniqKey="Zhou J" first="Jichun" last="Zhou">Jichun Zhou</name>
<affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="Aff2">Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</nlm:aff>
<wicri:noCountry code="subfield">310016 Zhejiang China</wicri:noCountry>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of Hematology & Oncology</title>
<idno type="eISSN">1756-8722</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
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</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Tamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Our findings demonstrate that H19 induces autophagy activation <italic>via</italic>
the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer.</p>
</sec>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (10.1186/s13045-019-0747-0) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Hematol Oncol</journal-id>
<journal-id journal-id-type="iso-abbrev">J Hematol Oncol</journal-id>
<journal-title-group><journal-title>Journal of Hematology & Oncology</journal-title>
</journal-title-group>
<issn pub-type="epub">1756-8722</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31340867</article-id>
<article-id pub-id-type="pmc">6657081</article-id>
<article-id pub-id-type="publisher-id">747</article-id>
<article-id pub-id-type="doi">10.1186/s13045-019-0747-0</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>The long noncoding RNA H19 promotes tamoxifen resistance in breast cancer <italic>via</italic>
autophagy</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Ji</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xie</surname>
<given-names>Shuduo</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yang</surname>
<given-names>Jingjing</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xiong</surname>
<given-names>Hanchu</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Jia</surname>
<given-names>Yunlu</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhou</surname>
<given-names>Yulu</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Yongxia</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ying</surname>
<given-names>Xiaogang</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Cong</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ye</surname>
<given-names>Chenyang</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Wang</surname>
<given-names>Linbo</given-names>
</name>
<address><email>linbowang@zju.edu.cn</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Zhou</surname>
<given-names>Jichun</given-names>
</name>
<address><email>jichun-zhou@zju.edu.cn</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Department of Surgical Oncology, Sir Run Run Shaw Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
No.3 Eastern Qingchun Road, Hangzhou, 310016 Zhejiang China</aff>
<aff id="Aff2"><label>2</label>
Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, 310016 Zhejiang China</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1759 700X</institution-id>
<institution-id institution-id-type="GRID">grid.13402.34</institution-id>
<institution>Cancer Institute (Key Laboratory of Cancer Prevention & Intervention, National Ministry of Education), Second Affiliated Hospital,</institution>
<institution>Zhejiang University School of Medicine,</institution>
</institution-wrap>
Hangzhou, 310009 China</aff>
</contrib-group>
<pub-date pub-type="epub"><day>24</day>
<month>7</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>24</day>
<month>7</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>12</volume>
<elocation-id>81</elocation-id>
<history><date date-type="received"><day>3</day>
<month>1</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>31</day>
<month>5</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s). 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>
) applies to the data made available in this article, unless otherwise stated.</license-p>
</license>
</permissions>
<abstract id="Abs1"><sec><title>Background</title>
<p id="Par1">Tamoxifen resistance remains a clinical challenge for hormone receptor-positive breast cancer. Recently, dysregulations in autophagy have been suggested as a potential mechanism for tamoxifen resistance. Although the long noncoding RNA H19 is involved in various stages of tumorigenesis, its role in tamoxifen resistance remains unknown. Here, we assessed the role of H19 in the development of tamoxifen-resistant breast cancer.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Quantitative real-time PCR analyzed expression of H19 in tamoxifen-resistant breast cancer tissues. Knockdown of H19 was used to assess the sensitivity to tamoxifen in vitro and in vivo. Both knockdown and overexpression of H19 were used to analyze the status of autophagy. Real-time quantitative methylation-specific polymerase chain reaction, chromatin immunoprecipitation, immunofluorescence, and Western blot were used to explore the tamoxifen resistance mechanism of H19.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">In this study, we observed that the expression of H19 was substantially upregulated in tamoxifen-resistant breast cancer cell line and tumor tissues, and knockdown of H19 enhanced the sensitivity to tamoxifen both in vitro and in vivo. Furthermore, knockdown of H19 significantly inhibited autophagy in MCF7 tamoxifen-resistant (MCF7/TAMR) cells. Conversely, overexpression of H19 promoted autophagy. Interestingly, overexpression of H19 in MCF7 tamoxifen-sensitive cells could recapitulate tamoxifen resistance. Moreover, an increase in methylation in the promoter region of Beclin1 was observed in MCF7/TAMR-shH19 cells. In the double knockdown groups, both shH19+shSAHH and shH19+shDNMT3B rescued the Beclin1 promoter region methylation levels and reactivated autophagy functions. A chromatin immunoprecipitation assay further validated that DNMT3B binds to the Beclin1 promoter region and the knockdown of H19 increases this binding.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Our findings demonstrate that H19 induces autophagy activation <italic>via</italic>
the H19/SAHH/DNMT3B axis, which could contribute to tamoxifen resistance in breast cancer.</p>
</sec>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (10.1186/s13045-019-0747-0) contains supplementary material, which is available to authorized users.</p>
</sec>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>LncRNA H19</kwd>
<kwd>Autophagy</kwd>
<kwd>Methylation</kwd>
<kwd>Beclin1</kwd>
<kwd>Breast cancer</kwd>
<kwd>Tamoxifen resistance</kwd>
</kwd-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
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